Effects of PM2.5 exposure on the Notch signaling pathway and immune imbalance in chronic obstructive pulmonary disease

Gu, Xing-yu; Chu, Xu; Zeng, Xiaoli; Bao, Hairong; Liu, Xiaoju

doi:10.1016/j.envpol.2017.03.070

Cited by 87 publications

(53 citation statements)

References 41 publications

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“…*p < 0.05; **p < 0.01 COPD patients exposed to ambient air pollution due to aggravation of the Th1/Th2 and Th17 imbalance. Our results were consistent with the findings of Gu et al who found that Th1, Th17, IFN-γ and IL-17 levels were increased in association with air pollution in COPD mice, while IL-4, IL-10, Th2 and regulatory T cells (Tregs) were significantly decreased compared with levels in the healthy group [34]. Therefore, PM 2.5 exposure aggravates Th1-and Th17-mediated immune disorders [34].…”

Section: Discussionsupporting

confidence: 93%

Lung function and systemic inflammation associated with short-term air pollution exposure in chronic obstructive pulmonary disease patients in Beijing, China

Gao

et al. 2020

Environ Health

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Background: Exposure to air pollution is associated with chronic obstructive pulmonary disease (COPD). However, findings on the effects of air pollution on lung function and systemic inflammation in Chinese COPD patients are inconsistent and scarce. This study aims to evaluate the effects of ambient air pollution on lung function parameters and serum cytokine levels in a COPD cohort in Beijing, China. Methods: We enrolled COPD participants on a rolling basis from December 2015 to September 2017 in Beijing, China. Follow-ups were performed every 3 months for each participant. Serum levels of 20 cytokines were detected every 6 months. Hourly ambient pollutant levels over the same periods were obtained from 35 monitoring stations across Beijing. Geocoded residential addresses of the participants were used to estimate daily mean pollution exposures. A linear mixed-effect model was applied to explore the effects of air pollutants on health in the first-year of follow-up. Results: A total of 84 COPD patients were enrolled at baseline. Of those, 75 COPD patients completed the first-year of follow-up. We found adverse cumulative effects of particulate matter less than 2.5 μm in aerodynamic diameter (PM 2.5), nitrogen dioxide (NO 2), sulfur dioxide (SO 2) and carbon monoxide (CO) on the forced vital capacity % predicted (FVC % pred) in patients with COPD. Further analyses illustrated that among COPD patients, air pollution exposure was associated with reduced levels of serum eotaxin, interleukin 4 (IL-4) and IL-13 and was correlated with increased serum IL-2, IL-12, IL-17A, interferon γ (IFNγ), monocyte displacing protein 1 (MCP-1) and soluble CD40 ligand (sCD40L). Conclusion: Acute exposures to PM 2.5 , NO 2 , SO 2 and CO were associated with a reduction in FVC % pred in COPD patients. Furthermore, short-term exposure to air pollutants increased systemic inflammation in COPD patients; this may be attributed to increased Th1 and Th17 cytokines and decreased Th2 cytokines.

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Section: Discussionsupporting

confidence: 93%

Lung function and systemic inflammation associated with short-term air pollution exposure in chronic obstructive pulmonary disease patients in Beijing, China

Gao

et al. 2020

Environ Health

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“…Meanwhile, PM2.5 has the feature of small volume, which can be inhaled and deposited in the alveolar, and can aggravate airway inflammation and immune response induced by COPD [ 5 ]. The immune disorder induced by PM2.5 is related to, but also aggravates, COPD [ 6 ]. Therefore, it is of significance to find treatment for COPD in the condition of PM2.5 exposure.…”

Section: Introductionmentioning

confidence: 99%

Effects of 1,25-Dihydroxyvitamin D3 on the Prevention of Chronic Obstructive Pulmonary Disease (COPD) in Rats Exposed to Air Pollutant Particles Less than 2.5 Micrometers in Diameter (PM2.5)

et al. 2018

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BackgroundThis study aimed to investigate the effects of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) on airway changes in chronic obstructive pulmonary disease (COPD) rats exposed to air pollutant particles less than 2.5 micrometers in diameter (PM2.5), and to evaluate the mechanisms.Material/MethodsThree groups were included in this study: a normal group, a COPD model group, and a COPD with 1,25(OH)2D3 treatment group. In each group, the rats were divided into four subgroups: control and different doses of PM2.5 (1.6, 8 and 40 mg/kg body weight). Apoptosis in lung tissue was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). The expression of c-Jun N-terminal kinase 1 (JNK1) and mucin 5AC (MUC5AC) were detected by real-time polymerase chain reaction (RT-PCR), Western blotting and immunofluorescence staining.ResultsCompared with corresponding subgroups in normal group, the apoptotic rates in COPD group were significantly increased. By contrast, 1,25(OH)2D3 treatment group significantly reduced COPD-induced apoptosis in lung tissue. Upon the dose increase of PM2.5, the apoptotic rate was also elevated in each group. Compared with the corresponding control in each group, PM2.5 increased apoptosis in a dose-dependent manner. Importantly, 1,25(OH)2D3 also prevented apoptosis in COPD rats exposed to PM2.5. Mechanically, the expression of MUC5AC and JNK1 in COPD group was significantly upregulated, compared with corresponding subgroups in the normal group. Treatment with 1,25(OH)2D3 reduced expression of MUC5AC and JNK1 in COPD rats. It was found that the expression of MUC5AC and JNK1 was elevated with the dose increase of PM2.5 in each group. Consistently, 1,25(OH)2D3 also reduced the expression of MUC5AC and JNK1 in COPD rats exposed to PM2.5.Conclusions1,25(OH)2D3 prevented lung injury in COPD rats with or without PM2.5 exposure. Our results suggest that 1,25(OH)2D3 is useful to mitigate the injury caused by COPD.

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“…Sub-chronic exposure to PM2.5 has also been indicated to induce inflammatory injury in rats and impair the phagocytic function of AM (alveolar macrophage) (98). Furthermore, PM2.5 has been demonstrated to increase the phagocytic ability of macrophages in mice with COPD, thus increasing oxidative stress (99). PM2.5 also impairs the immune balance of mice with COPD by blocking the Notch signaling pathway (99).…”

Section: Pm25-induced Inflammatory Response and Oxidative Stressmentioning

confidence: 99%

“…Furthermore, PM2.5 has been demonstrated to increase the phagocytic ability of macrophages in mice with COPD, thus increasing oxidative stress (99). PM2.5 also impairs the immune balance of mice with COPD by blocking the Notch signaling pathway (99). Exposing nasal mucosa epithelial cells to PM2.5 indicated that PM2.5 was able to increase ROS and Nrf2 levels, which have an association with oxidative stress (100).…”

Section: Pm25-induced Inflammatory Response and Oxidative Stressmentioning

confidence: 99%

Function of PM2.5 in the pathogenesis of lung cancer and chronic airway inflammatory diseases (Review)

2018

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Previous research has identified that air pollution is associated with various respiratory diseases, but few studies have investigated the function served by particulate matter 2.5 (PM2.5) in these diseases. PM2.5 is known to cause epigenetic and microenvironmental alterations in lung cancer, including tumor-associated signaling pathway activation mediated by microRNA dysregulation, DNA methylation, and increased levels of cytokines and inflammatory cells. Autophagy and apoptosis of tumor cells may also be detected in lung cancer associated with PM2.5 exposure. A number of mechanisms are involved in triggering and aggravating asthma and COPD, including PM2.5-induced cytokine release and oxidative stress. The present review is an overview of the underlying molecular mechanisms of PM2.5-induced pathogenesis in lung cancer and chronic airway inflammatory diseases.

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Effects of PM2.5 exposure on the Notch signaling pathway and immune imbalance in chronic obstructive pulmonary disease

Cited by 87 publications

References 41 publications

Lung function and systemic inflammation associated with short-term air pollution exposure in chronic obstructive pulmonary disease patients in Beijing, China

Lung function and systemic inflammation associated with short-term air pollution exposure in chronic obstructive pulmonary disease patients in Beijing, China

Effects of 1,25-Dihydroxyvitamin D3 on the Prevention of Chronic Obstructive Pulmonary Disease (COPD) in Rats Exposed to Air Pollutant Particles Less than 2.5 Micrometers in Diameter (PM2.5)

Function of PM2.5 in the pathogenesis of lung cancer and chronic airway inflammatory diseases (Review)

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